Endocrinology Flashcards

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1
Q

Diagnostic test thresholds for diabetes diagnosis

A

Random plasma glucose

  • PreDM 140-199
  • DM 200

Fasting plasma glucose

  • PreDM 100-125
  • DM 126

2-hour OGTT

  • PreDM 140-199
  • DM 200

HgA1c

  • PreDM 5.8-6.4%
  • DM 6.5%
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2
Q

Labs to distinguish type 1 from type 2 DM

A

C peptide

Antibodies:
Anti-insulin antibodies (IAA)
Anti-islet cell cytoplasm antibodies (ICA)
Anti-Glutamic acid decarboxylase antibodies (GAD) -MC
Anti-tyrosine phosphatase antibodies

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3
Q

Precipitating factors for DKA

A
Undiagnosed diabetes
Missed insulin doses
Infection - PNA, gastroenteritis, UTI
Severe medical illness - MI, stroke, bowel ischemia
Trauma
Medications - glucocorticoids
alcohol or drug abuse
Pancreatitis
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4
Q

DKA - features and diagnosis

A
Features:
Weakness
Polyuria and polydipsia
Abdominal pain, nausea, vomiting
Altered mental status -> coma
Kussmaul breathing - deep, labored, fast
Fruity order on breath
Dry mucous membranes
low skin turgor

Dx:
Glucose 200-600
High anion gap metabolic acidosis - ABG, BMP
Serum/urine ketones
Sodium +/- pseudohyponatremia
Potassium looks high - low total body K, excreted in urine

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5
Q

Treatment of DKA

A

Admit to ICU

IVF - NS or LR - large boluses - esp hypotension
IV insulin
Add IV glucose when glucose less than 200
Electrolyte management: potassium above 4, magnesium above 2, phosphorus, calcium
Identify and treat any precipitating factors

Wait until anion gap closes to stop insulin - bridge to subcutaneous insulin for maintenance

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6
Q

DKA vs HHS

A
DKA:
T1DM
Glucose over 200
pH less than 7.3
ketones present
High anion gap
Normal/variable plasma osmolality
HHS:
T2DM
Glucose over 600
pH >7.3
small or absent ketones
normal/variable anion gap

Plasma osmolality >320 (high)

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7
Q

Hyperosmolar hyperglycemic non-ketotic state

A

Features:
Polyuria and polydipsia
Dehydration
AMS, seizures, stroke, coma

Dx:
Glucose >600-800
No acidosis
elevated plasma osmolality (>320)

Tx:
Admit to ICU
IV insulin
Correct electrolytes
Identify and treat underlying disorder

End treatment: normalized glucose and osmolality

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8
Q

Nonproliferative diabetic retinopathy

A

Cotton wool spots
Hard exudates
Microaneurysms
Tortuous vessels

Tx: if severe - panretinal photocoagulation PRP

Surveillance and blood glucose and BP control

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9
Q

Proliferative diabetic retinopathy

A
Neovascularization - fragile new vessels prone to hemorrhage
Cotton wool spots
Hard exudates
Hemorrhage
AV nicking
Edema
Tx:
PRP
VEGF inhibitors
Intravitreal corticosteroid
Vitrectomy (if vitreous hemorrhage)
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10
Q

Diabetic nephropathy

A

Microalbuminemia ->
Overt proteinuria ->
Nephrotic syndrome and/or Progressive kidney dysfunction
-Kimmelstiel-Wilson nodules on pathology

-> hemodyalsis

Tx: prevention - ACE/ARB

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11
Q

Diabetic neuropathy

A

Sensory:

  • Progressive stocking/glove distribution
  • paresthesias, dysesthesias, or numbness
  • prevention of injury and infection is paramount

Motor

  • poor coordination
  • weakness

Autonomic

  • erectile dysfunction
  • postural hypotension
  • incontinence
  • gastroparesis (tx erythomycin, metoclopramide)

Tx:
Gabapentin, carbamazepine, pregabalin - nerve pain
TCAs, duloxetine
Narcotics, tramadol last resort

Goal: avoid injury/infection

Complications
Charcot joints - chronic progressive arthropathy
-associated with tabes dorsalis and diabetes

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12
Q

DM preventive care

A

HbA1c q3 mo -> q6 if stable at goal
urine microalbumin:cr ratio - over 300, get 24 hr urine

lipids q1 yr
-treat with mod-high intensity over 40

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13
Q

Complications from bypass surgery

A

Deficiencies of iron, B12, folate, thiamine, vitamin D
Dumping syndrome - bloating, swelling, cramping
GERD
Vomiting

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14
Q

Criteria for metabolic syndrome

A
Abdominal obesity
Elevated triglycerides
Low HDL
Elevated blood pressure
Abnormal blood glucose
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15
Q

Symptoms of hypoglycemia

A
Adrenergic symptoms (elevated epi)
Faintness
Weakness
Anxiousness
Sweating
Palpitations
-beta blockers can mask the symptoms
neuroglyopenic symptoms
Headache
Confusion
Mental status changes
Seizure
Loss of consciousness
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16
Q

Whipple’s Triad

A

Symptoms of hypoglycemia - especially after fasting or heavy exercise

Low plasma glucose - below 45 at time of symptoms

Relief of symptoms when the glucoses raised to normal

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17
Q

Reactive hypoglycemia

A

Excessive insulin production in response to the amount of blood glucose present

Occurs 1-3 hours after a high carb meal

Dx: mixed meals tolerance test instead of fasting to induced hypoglycemia

after gastric bypass or in prediabetes

Encourage high protein and less junk food

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18
Q

Insulinoma

A

Insulin secreting tumor are usually in the pancreas
Hypoglycemia while fasting

Get imaging CT/MRI to localize
Surgery if tumor identified

Diazoxide - inhibits insulin secretion
Octreotide

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19
Q

Secondary hypoglycemia to other disease

A

Liver disease, Malnutrition, adrenal insufficiency

Hypoglycemia during fasting

Dx:
Check LFTs
Markers of nutrition
Cortisol stimulation test
ACTH level
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20
Q

Alcohol induced hypoglycemia

A

Decreased gluconeogenesis - NADPH used up to metabolize alcohol

Hypoglycemia with fasting

Check the blood alcohol level

Give thiamine before glucose to prevent Wernicke encephalopathy

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21
Q

Thyrotropin releasing hormone (TRH)

A

Released from the hypothalamus

Stimulates TSH from pituitary

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22
Q

Thyroid stimulating hormone (TSH)

A

Released from pituitary gland
Stimulates the thyroid directly

Best test for thyroid function
Elevated in hypothyroidism
Changes exponentially with small changes in T4/T3

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23
Q

Thyroxine (T4)

A

Thyroid hormone
Replace to therapeutically in hypothyroidism
Half-life 7 to 10 days

Measure free T4 level
Low in hypothyroidism

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24
Q

Triiodothyronine (T3)

A

Thyroid hormone mostly produced in peripheral tissues
High affinity for receptor
Short half-life

Measure free T3 level
low in hypothyroidism

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25
Q

Thyroid binding globulin (TBG)

A

Protein that binds circulating T4 and T3
High in pregnancy and OCP use (high estrogen states)
Low in liver failure and nephrotic syndrome (low-protein states)

Amount of TBG affects total T4 and T3 levels, but not free levels

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26
Q

Thyroid peroxidase antibody (TPO)

A

Causative antibody (others: antithyroglobulin and antimicrosomal) in Hashimoto’s thyroiditis

Used to Determine cause of hypothyroidism

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27
Q

Causes of hypothyroidism

A
Congenital hypothyroidism
Hashimoto's thyroiditis
Iodine deficiency or excess
Subacute granulomatous thyroiditis (de Quervain)
Riedel's thyroiditis
Neck radiation - including treatment for hyperthyroidism with radioactive iodine
Surgical removal of the thyroid
Idiopathic causes

Medications:
Amiodarone - lots of iodine
Lithium
Tyrosine kinase inhibitors (imatinib)

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28
Q

Clinical features and treatment for hypothyroidism

A
Features:
Cold intolerance
Weight gain
Fatigue
Constipation
Voice hoarseness or change
Menorrhagia
Slowed mental or physical function
Dry skin with coarse brittle hair
Reflexes - slow return phase

Tx:
Levothyroxine - T4
Synthetic T3
Natural thyroid replacement - dosing inconsistencies

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29
Q

Hashimoto thyroiditis

A

Women - teens and middle age
Euthyroid state early in disease
Thyrotoxicosis d/t inflammation and destruction of follicle cells
-> painless goiter, hypothyroid

Dx:
Elevated total and LDL cholesterol - recovers as treated
Thyoid peroxidase (TPO), antithyroglobulin and antimicrosomal Abs

Tx: thyroid hormone replacement

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30
Q

Subacute thyroiditis

A
Features:
PAINFUL goiter
neck pain
Fever
Elevated ESR
Low uptake on thyroid scan

Cause hyper or hypothyroidism

Tx:
NSAIDS, steroids - pain
replace thyroid hormone if hypo
Bet-blockers if hyper
continue to monitor thyroid levels
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31
Q

Riedel’s Thyroiditis

A

Young
Fixed, hard, rock like, painless thyroid
Fibrosis extends into adjacent structures

Euthyroid or hypothyroidism

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32
Q

Congenital hypothyroidism

A

Causes:
Sporadic thyroid dysgenesis
Severe iodine deficiency
Hereditary disorder of the thyroid hormone synthesis

Features:
Lethargy
Poor feeding
Thick, protruding tongue
Constipation
Umbilical hernia
Moderate to severe intellectual disability
Maternal hormones can cross placenta - normal intrauterine development

Dx:
Newborn screen TSH

Tx: replace hormone

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33
Q

Causes of hyperthyroidism

A

Graves dz
Toxic adenoma
Toxic multinodular goiter -> obstructive sxs

34
Q

Toxic adenoma

A

“hot nodule”
hyperfunctioning nodule takes up more iodine than surrounding tissue

single or multiple (toxic multinodular goiter)

35
Q

Graves Disease

A

autoimmune
Stimulates TSH receptor
TSI Ab

Features:
painless goiter +/- thyroid bruits
Exophthalamos - dry eyes, abnormal EOM exam
Pre-tibial myxedema

Dx:
Low TSH - usually totally suppressed
Free elevated T4 and T3
+/- elevated TSI Ab

36
Q

Thyrotoxicosis

A

Elevated thyroid hormone levels from thyroiditis
iatrogenic: wrong dose (accidental or intentional)
Meds with high iodine: amiodarone, IV contrast

Features:
wt loss
increased appetite
heat intolerance
sweating
anxiety
difficulty sleeping
palpitations
bowel hypermobility
Exam:
tremors
sinus tachycardia
elevated pulse pressure
warm skin
hyper reflexia
Afib

Long standing: CHF, Fx osteoporosis, death

37
Q

Treatments for hyperthyroidism

A

Thionamide medications - Methimazole, propylthiouracil
Thyroidectomy
Radioactive iodine
B-blocker for sxs management

38
Q

Causes of thyroiditis

A

Viral infection
Subacute (de Quervain, granulomatous) thyroiditis
Postpartum thyroiditis

39
Q

Postpartum thyroiditis

A

silent
painless goiter
lower uptake on thyroid scan

Dx:
TSI Ab - rule out graves activation
Radioactive iodine - if not breast feeding

Tx: self limited, tx sxs

40
Q

thyroid storm

A

almost always Graves disease - untreated
high mortality rate

Features:
tachycardia - >140 -> sweating
hyperpyrexia >103F
AMS, LOC
GI: N/V/D
Tremor
Warm, sweaty skin
Goiter
Eye: lid lag, proptosis, ophthalmopathy (in Graves)

Labs: low TSH, high free T4/T3

Tx:
B-blockers - control adrenergic tone
Thionamides - block synthesis/conversion
IV potassium iodide - block release of thyroid hormone
Glucocorticoids - decrease T4-> T3 conversion
ICU admit - stabilize
Once Stable -> radioactive iodine

41
Q

Thyroid nodules

A

Extremely common
4-6% solitary cancerous
Hyper functioning nodules never malignant

Cancer risk factors:
Age less than 30, >60 yo
Hx of neck radiation
Smoking
FHx of thyroid cancer
US characteristics predictive of malignancy:
Hypoechoic
Irregular margins
Microcalcifications
Taller than wide
42
Q

Management of thyroid nodule

A

Check TSH and thyroid US

Hyperthyroid -> radionuclide uptake and scan

  • HOT nodule -> treat as hyperthyroid
  • COLD nodule -> FNA

Hypothyroid or euthyroid -> +nodule go to FNA, no nodule FNA not indicated

43
Q

Thyroid FNA cytology follow up

A

Nondiagnostic -> repeat FNA
Benigh -> surveillance
Indeterminant -> gene expression analysis vs surgery
Malignant or suspicious for malignancy -> surgery

44
Q

Papillary carcinoma of thyroid

A
MC 
younger
No hematogenous spread
Mets to LN of neck
Slow growing
Excellent prognosis
Tx:
Total thyroidectomy
\+/- LN dissection
\+/- radioactive iodine - large dose
-large tumor, LN involvement
45
Q

Follicular carcinoma of thyroid

A

slow moving, treatable
follicular structure
hematogenous spread

Tx:
Total thyroidectomy
\+/- LN dissection
\+/- radioactive iodine - large dose
-large tumor, LN involvement
46
Q

Medullary carcinoma of thyroid

A

CA of parafollicular cells
Screen for Pheo before surgery - assoc w/ MEN II
Screen RET oncogene

Tx:
Surgery
does not respond to radioactive iodine
Follow calcitonin levels for remission

47
Q

Anaplastic carcinoma of thyroid

A
undifferentiated
older patients
rock hard
rapidly growing
rapidly fatal

Tx:
surgical +/- radioactive iodine
-not efficiently making thyroid hormone or using iodine

48
Q

Chemos used for unresectable thyroid tumors

A

tyrosine kinase inhibitors

Levothyroxine to decrease TSH, slow growth

49
Q

Risk of thyroidectomy

A

hoarseness - damage recurrent laryngeal n

hypoparathyroidism and tetany
Tx - calcitriol, Ca, Mg

50
Q

Parathyroid hormone activity

A

Increase osteoclast activity
Increase distal tubule Ca2+ reabsorption
decrease phosphate reabsorption “Phosphate Trashing Hormone”
increase 1-alpha-hydroxylase activity in kidney - 25-OH Vit D to 1,25 OH Vit D -> intestinal absorption of calcium, resorb phosphate renal prox tubule

51
Q

Consequences of hypercalcemia

A

MC - asx

“Bones, Stones, Groans, Psych overtones”

Bones - pain, osteoporosis, Fx, osteitis fibrosa

Stones: renal stones, nephrocalcinosis

Goans - C/V/N, PUD (elevated gastrin d/t high cal), pancreatitis

Psych: lethargy, fatigue, depression, memory loss, personality change, confusion, stupor coma

Other: proximal m. weakness, keratitis, conjunctivitis, HTN, itching

52
Q

Primary hyperparathyroidism

A

Causes:
Single adenoma (MC)
Hyperplasia (one or more gland)
Parathyroid cancer (rare)

Dx:
high calcium
low phosphate
high or normal PTH
high urine calcium
\+/- elevated alk phos
DEXA - decreased bone density
Localize gland with US vs sestimibi

Surgical Tx:
Adenoma - remove gland, check intraoperative PTH
Hyperplasa - remove 3 1/2 glands, mark remaining with clip or transplant to forearm

Medical:
Cinacalcet - increases sensitivity of Ca-R on parathyroid, lowers PTH
Avoid thiazides (retain Ca) and lithium (raises PTH)
Hydration - polyuria from hypercalcemia -> fluid loss
Biphosphonates
minimize fall risks
Routine monitoring - serum Ca, Cr, bone density

53
Q

Indications for surgical parathyroidectomy in primary hyperthyroidism

A

hypercalcemia sxs
serum Ca > 1.0 above upper limit of normal
Cr clearance less than 60
less than -2.5 T score at any sight - forearm thins faster
Under 50 yo

54
Q

Treatment for hyperparathyroidism due to chronic renal disease

A

Tx hyperphosphatemia

  • oral binders - calcium carbonate, calcium acetate, and/or sevelamer
  • NOT citrate - binds aluminum

Prevent renal osteodystrophy

  • calcitriol
  • may require cinacalcet to suppress PTH secretion
55
Q

hyperparathyroidism d/t chronic renal disease

A

PTH high due to:

  • elevated FGF23 -> low alpha hydroxylase in kidney - no Vit D activation
  • elevated phosphate - can’t excrete

Causes osteomalacia or renal osteodystrophy

Tx like primary

56
Q

Hypoparathyroidism

A

Causes:
surgical parathyroidectomy
Autoimmune destruction

Hypocalcemia Sxs:
tingling lips/fingers
paresthesias
carpal/pedal spasms
Severe -> tetany, laryngeal spasm, seizures

Chvostek’s sign - check
Trousseau’s sign

Dx:
Low Ca, low PTH
High phosphate
High bone density - but more fx d/t abnormal architecture

Tx:
calcitriol, 1-25 OH D3

57
Q

Pseudohypoparathyroidism

A

Tissue non-repsonsive to PTH at receptor level

AD - GNAS-1 gene mutation

  • maternal imprinting
  • Mom gene -> full disease - Albright’s + hypocalcemia
  • Dad gene -> partial disease - Albrights with no hypocalcemia
Albright's hereditary osteodystrophy (AHO)
Short stature
Short 4th metacarpal
developmental delay
obesity

Dx:
Low Ca
High PTH
High phosphate

Tx: Calcium/Vit D supplementation

58
Q

Drugs linked to hyperprolactinemia

A

phenothiazines - Risperidone, Haloperidol
Methyldopa
Verapamil

59
Q

Treatment of prolactinoma

A

1st: DA agonist - cabergoline > bromocriptine
If fail -> transphenoidal surgery
If large, radiation after surgical debulking

60
Q

Acromegaly

A

average onset to dx is 12 yrs

Features:
enlargement of jaw (teeth spread apart), nose, frontal bones (coarse facial features), hands/feet (increase in ring, glove, shoe size)

Soft tissue growth - voice deepens, macroglossia (teeth indentations in tongue), carpal tunnel syndrome, other entrapment syndromes, hypertrophy of synovial tissue and cartilage _. arthropathy, spinal cord compression if vertebrae involved

CV: HTN, LVH, diastolic dysfunction

Glucose intolerance -> DM

Increased organ size - spleen, liver, kidneys

Vision loss d/t optic chiasm compression from tumor

Tests:
IGF-1
Confirm with oral glucose suppression test
-75 g glucose -> measure GH at 1 hr and 2 hrs -> GH concentration >1 ng/mL = acromegaly

Positive test -> pituitary MRI - mass or empty sella

Tx:
Transsphenoidal resection or external beam radiation
Octreotide or lanreotide - inhibits GH secretion
If somatostatin analog fails -> cabergoline (Bromocriptine less effective)
If cabergoline fails -> pegvisomant (GH receptor antagonist)

Follow IGF 1 level

61
Q

Adrenal cortex

A

Glomerulosa - mineralocorticoids - aldosterone

Fasciculata - glucocorticoids - cortisol

Reticularis - androgens (testosterone, DHEA-S)

62
Q

Causes of Cushing syndrome

A

High ACTH:

  • pituitary adenoma producing ACTH (Cushing disease)
  • Ectopic production of ACTH (small cell lung cancer, carcinoid tumor)

Low ACTH:
Exogenous steroid medications (MC)
Adrenal adenoma or hyperplasia

63
Q

Cushing syndrome symptoms

A

“BAM CUSHINGOID”

Buffalo hump
Amenorrhea
Moon facies
Clots (thrombotic), Cardiac disease, Crazy (psychosis, agitation)
Ulcers (peptic)
Skin (striae, acne, easy bruising)
Hypertension, Hypokalemia, Hirsuitism
Infection
Necrosis of the femoral head
Glaucoma and cataracts (eye problems)
Osteoporosis
Immune suppression
Diabetes
64
Q

Long term complications of Cushing Syndrome

A
thormboembolic disease
CV disease - mortality cause
HTN, electroylte abnormalities
Infection risk
osteoporosis
Avascular necrosis of hip
DM - hard to control
65
Q

Diagnostic evaluation of Cushing syndrome

A

Measure ACTH->

-Low - ACTH independent Cushings-> adrenal imaging

-Intermediate (normal) - get CRH test
no response -> adrenal imaging
elevated ACTH and cortisol -> ACTH dependent Cushings

-High - ACTH dependent Cushings -> pituitary MRI
Tumor - Inferior petrosal sinus sampling (IPSS) for lateralization/confirmation
No tumor - IPSS for central vs peripheral
-Central levels higher - pituitary source
-Central levels same as peripheral -> Body scan for ectopic source OR High dose dexamethasone test or CRH test

High dose dexamethasone

  • if suppresses ACHT/Cortisol - likely pituitary source, “woke up” feedback loop
  • if no suppression then ectopic source
66
Q

Treatment of cushing syndrome

A

Limit exogenous steroids

If tumor - remove
-consider repeat surgery if initial surgery unsuccessful

Pituitary source - radiation to sella if surgery not possible

Mifepristone - blocks cortisol receptors for refractory or inoperable Cushing syndrome with hyperglycemia

Ectopic - treat underlying disease

67
Q

Triad of hyperaldosteronism

A

Hypertension
hypokalemia
metabolic alkalosis

68
Q

Primary Hyperaldosteronism (Conn syndrome)

Aldosterone:
Renin:
Aldosterone/Renin:

Cause
Treatment

A

Aldosterone: high
Renin: low
Aldosterone/Renin: high

Cause:
Adrenal adenoma
Bilateral hyperplasia

Treatment:
Remove adenoma OR spironolactone

69
Q

Secondary hyperaldosteronism

Aldosterone:
Renin:
Aldosterone/Renin:

Cause
Treatment

A

Aldosterone: high
Renin: high
Aldosterone/Renin: low

Cause:
Renal artery stenosis
CHF
Nephrotic syndrome
Cirrhosis
(Kidney senses low BP/hypoperfusion)

Treatment:
Treat underlying cause OR spironolactone

70
Q

Non-aldosterone mineralocorticoid hyperaldosteronism

Aldosterone:
Renin:
Aldosterone/Renin:

Cause
Treatment

A

Aldosterone: low
Renin: low
Aldosterone/Renin: low

Cause:
Cushing syndrome
Licorice ingestion ( enzyme blocks conversion of cortisol -> cortisone; aldosterone receptors stimulated)

Treatment:
Treat Cushing syndrome
STOP EATING LICORICE!

71
Q

Primary adrenal insufficiency (Addison’s dz)

Affected gland:
Causes:
ACTH:
Glucocorticoid deficiency:
Mineralocorticoid deficiency:
A

Affected gland: adrenal cortex

Causes:
Autoimmune (MC)
Infection (TB)
Hemorrhage

ACTH: very high
Glucocorticoid deficiency: yes
Mineralocorticoid deficiency: yes

(no rise of cortisol with cosyntropin (ACTH analog) stim test)

72
Q

Secondary adrenal insufficiency

Affected gland:
Causes:
ACTH:
Glucocorticoid deficiency:
Mineralocorticoid deficiency:
A

Affected gland: pituitary (pan-hypo)

Causes:
Surgery
Tumor
Hemorrhage
Autoimmune

ACTH: low
Glucocorticoid deficiency: yes
Mineralocorticoid deficiency: no

73
Q

Tertiary adrenal insufficiency

Affected gland:
Causes:
ACTH:
Glucocorticoid deficiency:
Mineralocorticoid deficiency:
A

Affected gland: Hypothalamus (lack CRH)

Causes:
Exogenous steroid administration

ACTH: low
Glucocorticoid deficiency: yes
Mineralocorticoid deficiency: no

74
Q

Labs and treatment for adrenal insufficiency

A
low Na
high K
eosinophilia
low cortisol
high ACTH (primary)
Low ACTH (secondary and tertiary)

Tx:
Treat underlying disease
glucocorticoids: hydrocortisone, dexamethasone, prednisone
Mineralocorticoids - Addison’s: Fludrocortisone
-need more cortisol during stress

75
Q

Adrenal (Addisonian) crisis

A
S/s:
shock
severe weakness
Fever 
AMS
Vascular collapse

Acute onset adrenal insufficiency (infarction or acute b/l adrenal hemorrhage)

Tx:
Fludrocortisone with high dose hydrocortisone (IV)
Electrolyte management - potassium drops fast with fludrocortisone replacement, high sodium
IVF if hypotensive
IV glucose
Vasopressors if needed for shock

76
Q

11 B hydroxylase deficiency

A

high androgens -> virilization of girls

High DOC -> HTN

77
Q

17 alpha hydroxylase deficiency

A
only aldosterone -> very very high levels
HTN
Ambiguous genitalia in boys
Amenorrhea later in girls
high Na, low androgens
78
Q

21 alpha-hydroxylase

A

mineralocorticoid deficiency -> hypotension, low Na, high K - salt wasting

High androgens -> virilization and ambiguous genitalia in girls

79
Q

Pheochromocytoma

A
Episodic
Palpitations with episodic tachycardia
CP
Diaphoresis with pallor
Headach
Anxiety
Episodic (labile) BP

Dx:
24 hr urine catecholamines - metanephrine, normetanephrin, VMA

Tx:
resect - pretreat with alpha blocker - phenoxybenzamine or phentolamine; then beta blocker
Can use carvedilol or labetalol

80
Q

MEN syndromes

A

MEN1 (PPP):
Parathyroid
Pituitary
Pancrease

MEN2a (PPM):
Parathyroid
Pheo
Medullary thyroid cancer

MEN2b (PMM):
Pheo
Medullary thyroid cancer
Mucosal neuromas

MEN2: RET